Sixty-four children with various types of acute leukemia who had received no prior treatment were treated with vincristine and prednisolone.
Fifty-five attained complete remission and one achived good partial remission.
For maintenance therapy, patients who attained remission were randomized into 2 groups; one received 6-mercaptopurine alone and the other received a combination of daily 6-mercaptopurine and consolidation therapy by “VAMP” regimen every three months.
The average duration of hematological remission in these groups was 7.0 and 17.9 months, respectively. Central nervous system leukemia developed in 22 of 64 patients.
The combination of vincristine and prednisolone was effective for remission induction of acute childhood leukemia.

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Ultrastructural changes of platelet granules in an early stage of platelet aggregation were observed, and localization of acid phosphatase was traced simultaneously.
In an early stage of platelet aggregation platelets lost their discoid shape, became irregularly spherical with multipe pseudopodial projections. Alpha granules grouped in the cell centers and appeared in the matrix homogeneous with decreased electron density. Subsequently various autophagic changes were observed in alpha granules.
The localization of acid phosphatase was observed within alpha granules. Acid phosphatase in alpha granules were activated simultaneously with starting of aggregation process. Reaction products were indicated in alpha granules which had increased electron density with homogeneous or granular structure. According to the lysosome concept these granules seemed to be the secondary lysosome. Autophagic process was also observed in larger vacuoles presumably resulted from fusion of granules. Autophagic vacuoles in various stages and their fragment were observed out of platelets in results of release reaction.
The results of these experiments presented that platelet granules possessed a character as lysosome and release reaction might be connected with activation of platelet lysosomal enzyme.

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Fifteen cases of chronic lymphocytic leukemia during the past seven years have been reported and incidence, clinical manifestation, treatment and prognosis were discussed.
The results were as follows.
1) The incidence was approximately 10 percent of all leukemias. The 15 patients consisted of 6 males and 9 females. All were adults with the mean age of 57.7 at onset.
2) Initial symptoms in 8 cases were enlarged lymph nodes, splenomegaly and bleeding tendency which were specific signs of C. L. L, but in other 7 cases the diagnosis of C. L. L. was disclosed by routine hematologic examination. By the initial physical findings of the C. L. L., these cases were divided into four categories: classic type 10 cases, splenomegalic 1 case, specific skin lesions 2 cases, and blood changes-only 2 cases.
Several immunological disturbances such as hemolytic anemia with eosinophilia, progressive vaccinia, runting syndrome and various seven infections were recognized. The low level of lyphocyte blastoid transformation with PHA or PWM, negative tuberculin reaction and hypogammaglobulinemia were also observed.
3) In most cases, hemoglobin and platelet count levels were within normal limit by initial hematological data. The peripheral leukocyte count was between 30,000 and 100,000 per cmm. Sixty to 99% of these cells were mature lymphocytes which are compatible with normal small lymphocytes.
4) Of these 14 cases, were treated with chlorambucil, corticosteroid and vincristine by combination method or alone. The effect of the treatment in 13 cases was evaluated as excellent in 4, good in 5 and slight to none in 4.
5) Five years survival rate of these 15 cases was 49.2%.

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In this repot we described a patient with gastric carcinoma associated with dicloncal gammopathy (IgG-K, IgG-L). This case showed following two characteristics. First, the levels of the two M-components changed each other during the course of the disease: this may perhaps be significant in considering M-components as antibodies produced in an immune response to components of the neoplastic tissue. Second, the gastric adenocarcinoma and its metastatic sites, mainly in lymph nodes and bone marrow, were markedly surrounded by plasma cells. Through the analysis of this case we discussed the relation between carcinoma and M-component and the significant of diclonal gammopathy.

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A thirty-six-year old woman was admitted to the Akita University Hospital on March, 1972.
One year before admission, she was diagnosed as agnogenic myeloid metaplasia of the spleen in the Akita Red Cross Hospital, because of marked splenomegaly, hepatomegaly, leukoerythroblastic anemia with tear drop poikilocyte, thrombocytopenia and hyperplastic bone marrow. Thereafter, her bone marrow became punctata sicca gradually.
After admission, she complained of repeated epistaxis and severe pain on the spleen area. The anemia progressed, so that a quantity of blood transfusion was necessary.
Splenectomy performed in November, 1972. The spleen weight 2,590 g.
After removal of spleen, her general condition and hematological data improved markedly.
A half year after splenectomy, she is in good condition with gain of 10 kg body weight, and with normal number of thrombocyte and moderate anemia.

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A 68-year-old man with generalized lymphadenopathy and hypergammaglobulinemia was reported.
The patient had an episode of fever 2 months prior to admission. After the fever subsided, the cervical lymphadenopathy developed, and became generalized about 2 months later. Superior vena caval syndrome was also found. On admission the patient was afebrile and slightly anemic. There was hepatomegaly, but no splenomegaly. The white cell count was 8200, with 6 per cent atypical lymphocytes. Plasma cells and atypical lymphocytes were moderately increased in the bone marrow. Serum electrophoresis showed increased polyclonal gammaglobulin level (4.9 g/dl). Cervical lymph node biopsy revealed reactive lymphoid and reticulum cell hyperplasia, without any evidence of malignancy. The titers of heterophil antibody, EB virus antibody, toxoplasma hemagglutinin, and cold agglutinin were all insignificant.
The lymphadenopathy and hypergammaglobulinemia disappeared with treatment of prednisolone. Three months after discontinuation of this treatment, he was perfectly well and free of all abnormalities.
Pathogenesis of this lymphadenopathy was briefly discussed as compared with lymphoreticulosis hyperglobulinemica.

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A case of microangiopathic hemolytic anemia associated with disseminated intravascular coagulation was reported.
A 44-year-old male, who had total gastrectomy in February 1971, complained of gingival bleeding since November 1972. He was admitted to our hospital because of the above complaint and severe hemolytic anemia. In the blood smear many abnormal red cells, such as helmet cells, burr cells, spherocytes and so on were observed. The coagulation studies have also revealed the decreased coagulative factors and activated fibrinolysis. The patient died suddenly of cerebral hemorrage. Autopsy was not permitted.
Although no clinical evidence suggestive of metastatic lesions was found before death, marked increase in alkaline phosphatase activity with its characteristic isozyme pattern has strongly suggested carcinomatous matastasis, which might have induced MHA as a trigger of formation of microthrombi.

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